Zobrazeno 1 - 10
of 12
pro vyhledávání: '"Malgorzata A. Mis"'
Autor:
Jianying Huang, Malgorzata A. Mis, Brian Tanaka, Talia Adi, Mark Estacion, Shujun Liu, Suellen Walker, Sulayman D. Dib-Hajj, Stephen G. Waxman
Publikováno v:
Scientific Reports, Vol 8, Iss 1, Pp 1-13 (2018)
Abstract Sodium channel Nav1.7 plays a central role in pain-signaling: gain-of-function Nav1.7 mutations usually cause severe pain and loss-of-function mutations produce insensitivity to pain. The Nav1.7 I234T gain-of-function mutation, however, is l
Externí odkaz:
https://doaj.org/article/8eca63acbcfb47469d32f11de63ac492
Autor:
Aristos J Alexandrou, Adam R Brown, Mark L Chapman, Mark Estacion, Jamie Turner, Malgorzata A Mis, Anna Wilbrey, Elizabeth C Payne, Alex Gutteridge, Peter J Cox, Rachel Doyle, David Printzenhoff, Zhixin Lin, Brian E Marron, Christopher West, Nigel A Swain, R Ian Storer, Paul A Stupple, Neil A Castle, James A Hounshell, Mirko Rivara, Andrew Randall, Sulayman D Dib-Hajj, Douglas Krafte, Stephen G Waxman, Manoj K Patel, Richard P Butt, Edward B Stevens
Publikováno v:
PLoS ONE, Vol 11, Iss 4, p e0152405 (2016)
Human genetic studies show that the voltage gated sodium channel 1.7 (Nav1.7) is a key molecular determinant of pain sensation. However, defining the Nav1.7 contribution to nociceptive signalling has been hampered by a lack of selective inhibitors. H
Externí odkaz:
https://doaj.org/article/b9af198893454af186b55747950a6251
Autor:
Mark Estacion, Lubin Chen, Malgorzata A. Mis, Shujun Liu, Betsy R. Schulman, Brian S. Tanaka, Jun-Hui Yuan, Sulayman D. Dib-Hajj, Stephen G. Waxman, Fadia B. Dib-Hajj
Publikováno v:
Brain Communications
There is a pressing need for understanding of factors that confer resilience to pain. Gain-of-function mutations in sodium channel Nav1.7 produce hyperexcitability of dorsal root ganglion neurons underlying inherited erythromelalgia, a human genetic
Autor:
Elizabeth J. Akin, Stephen G. Waxman, Malgorzata A. Mis, Fadia B. Dib-Hajj, Talia Adi, Brian S. Tanaka, Sulayman D. Dib-Hajj, Shujun Liu, Grant P. Higerd
Publikováno v:
Science Advances
Dynamic single-molecule imaging reveals NaV1.7 distribution and microtubule-dependent vesicular trafficking in sensory axons.
Sodium channel NaV1.7 controls firing of nociceptors, and its role in human pain has been validated by genetic and func
Sodium channel NaV1.7 controls firing of nociceptors, and its role in human pain has been validated by genetic and func
Publikováno v:
Trends in Pharmacological Sciences. 39:258-275
Chronic pain is a global unmet medical need. Most existing treatments are only partially effective or have side effects that limit their use. Rapid progress in elucidating the contribution of specific genes, including those that encode peripheral vol
Autor:
Yang Yang, Rolando Garcia-Milian, Brian S. Tanaka, Sulayman D. Dib-Hajj, Malgorzata A. Mis, Talia Adi, Carolina Gomis-Perez, Shujun Liu, Stephen G. Waxman, Fadia B. Dib-Hajj, Betsy R. Schulman
Pain is a complex process that involves both detection in the peripheral nervous system and perception in the CNS. Individual-to-individual differences in pain are well documented, but not well understood. Here we capitalized on inherited erythromela
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::668fbb95490d7501ba4ac7b3b6bb43af
https://europepmc.org/articles/PMC6335750/
https://europepmc.org/articles/PMC6335750/
Autor:
Sulayman D. Dib-Hajj, Talia Adi, Stephen G. Waxman, Mark Estacion, Shujun Liu, Brian S. Tanaka, Suellen M. Walker, Malgorzata A. Mis, Jianying Huang
Publikováno v:
Scientific Reports
Scientific Reports, Vol 8, Iss 1, Pp 1-13 (2018)
Scientific Reports, Vol 8, Iss 1, Pp 1-13 (2018)
Sodium channel Nav1.7 plays a central role in pain-signaling: gain-of-function Nav1.7 mutations usually cause severe pain and loss-of-function mutations produce insensitivity to pain. The Nav1.7 I234T gain-of-function mutation, however, is linked to
Publikováno v:
Trends in pharmacological sciences. 39(3)
Chronic pain is a global unmet medical need. Most existing treatments are only partially effective or have side effects that limit their use. Rapid progress in elucidating the contribution of specific genes, including those that encode peripheral vol
Autor:
Yang Yang, Sulayman D. Dib-Hajj, Lawrence J. Macala, Mark Estacion, Daniel B. Horton, Palak Shah, Stephen G. Waxman, Betsy R. Schulman, Malgorzata A. Mis, Jianying Huang
Publikováno v:
The Journal of neuroscience : the official journal of the Society for Neuroscience. 36(28)
Voltage-gated sodium channel Nav1.7 is a central player in human pain. Mutations in Nav1.7 produce several pain syndromes, including inherited erythromelalgia (IEM), a disorder in which gain-of-function mutations render dorsal root ganglia (DRG) neur
Autor:
Edward B. Stevens, Zhixin Lin, Anna Wilbrey, Stephen G. Waxman, Peter J. Cox, Sulayman D. Dib-Hajj, Mark L. Chapman, Malgorzata A. Mis, Christopher William West, R. Ian Storer, Stupple Paul Anthony, Elizabeth C. Payne, Manoj K. Patel, David Printzenhoff, Andrew D. Randall, James A. Hounshell, Douglas S. Krafte, Jamie Turner, Nigel Alan Swain, Aristos J. Alexandrou, Richard P. Butt, Adam R. Brown, Mark Estacion, Brian E. Marron, Alex Gutteridge, Neil A. Castle, Rachel Doyle, Mirko Rivara
Publikováno v:
PLoS ONE, Vol 11, Iss 4, p e0152405 (2016)
PLoS ONE
PLoS ONE
Human genetic studies show that the voltage gated sodium channel 1.7 (Nav1.7) is a key molecular determinant of pain sensation. However, defining the Nav1.7 contribution to nociceptive signalling has been hampered by a lack of selective inhibitors. H